With respect to possible treatment of the hyperinflammatory conditions in cystic fibrosis, “in vitro” experiments using CF cell lines and “in vivo” studies on CFTR-knockout mice demonstrated that PTL reduces inflammation by inhibiting NFκB activation, thereby decreasing the production of pro-inflammatory mediators, such as IL-8, the most relevant chemokine in CF [32]. This evidence concerns the gene NFKB1 and cystic fibrosis.